Do MEs cause CFS?

[JalapenoLuv]

So insulin would be a dead end for diabetes, JalapenoLuv? I think I am prepared to give methylation a bit more consideration than that.

Yes insulin is a dead end for diabetes. Look at what insulin therapy resulted in, delaying the search for the real underlying causes of type 2 diabetes. I never said I was against palliative care but when most of the health care system is based on maintenance type therapies to generate profits for pharmaceutical companies we have a problem.

I wonder if NIH is even funding non-palliative CFS research in any serious capacity. Their history isn't good.

And since we do not understand the role of bacteria and viruses, if any, I don't think I am persuaded any more in that direction.

I don't know about you but I understand the role of bacteria and viruses. I know what nagalase does. I understand the apoptotic pathways and the literature showing how certain bacteria disrupt them to parasitize cells. Start reading.

I do not do that protocol but I do not see why treating a disfunctional system can not help the immune system to fight intracellulair infections.

When the underlying infections aren't being stopped and if they block the immune response then the effect of treating a secondary problem is very limited. And it can't cure the disease.

 

[JalapenoLuv]

Methylation also doesn't make sense as an etiology. People are humming along just fine until they get a viral infection then suddenly their cells can't methylate properly? So what's the cause? It can't be environmental or infectious because nobody else is affected. It obviously isn't genetic because they didn't have it previously. It's a stupid theory out of desperation.

 

[lansbergen]

When the underlying infections aren't being stopped and if they block the immune response then the effect of treating a secondary problem is very limited. And it can't cure the disease.

Well there is no test and no treatment for the infection I suspect but using an immunemodulator gave me huge improvement .Lately it goes fast and even my lungs are healing now.

 

[JalapenoLuv]

Viruses are commonly found. Bacteria are tougher to find. I spoke to Ed Breitswerdt PhD from NC State who heads galaxy labs and he says his three day bartonella screen can now pick up bartonella spp. aka bartonella like organism which a previous version of the test previously missed.

Fluge did a study in 2011 which showed a statistically significant response in 10% of patients using the antibody Rituximab. I wonder if the reason why immunomodulators like rituximab help is if an infection is present then depleting the T cells would reduce the energy expenditure which otherwise would be used to build T cells and mount whatever response the body could do. Anyway, with only a 10% response rate it isn't going to make it to clinical practice.

 

[Sidereal]

Rituximab depletes B cells not T cells and the study showed that two-thirds of patients improved not 10%.

 

[JalapenoLuv]

You're right about the B cells (macrophages), but it doesn't matter. Both are involved.

Only 10% had statistically significant clinical response (3 out of 30 patients). You are confusing this with self reported fatigue questionnaires.

"Chronic fatigue syndrome (CFS) is a disease of unknown aetiology. Major CFS symptom relief during cancer chemotherapy in a patient with synchronous CFS and lymphoma spurred a pilot study of B-lymphocyte depletion using the anti-CD20 antibody Rituximab, which demonstrated significant clinical response in three CFS patients."
Benefit from B-Lymphocyte Depletion Using the Anti-CD20 Antibody Rituximab in Chronic Fatigue Syndrome. A Double-Blind and Placebo-Controlled Study.

 

[MeSci]

Fluge did a study in 2011 which showed a statistically significant response in 10% of patients using the antibody Rituximab. I wonder if the reason why immunomodulators like rituximab help is if an infection is present then depleting the T cells would reduce the energy expenditure which otherwise would be used to build T cells and mount whatever response the body could do. Anyway, with only a 10% response rate it isn't going to make it to clinical practice.

As someone else has pointed out, you have the facts wrong about this trial. You may find this thread interesting, especially in light of your apparent lack of knowledge about who @Jonathan Edwards is!

 

[JalapenoLuv]

Rituximab would be another dead end. Although initially their fatigue would be better, B cells serve a purpose and their long term clinical outcomes wouldn't be any better. In fact, with their fatigue masked they might be worse because they are overtasking their bodies beyond their recuperative abilities.

But if the funding is there and if he doesn't have anything better to do go for it.

 

[Marco]

@JalapenoLuv

Do you have hard information on something you'd like to share with us because you seem to know something that the rest us don't?

 

[JalapenoLuv]

I would but I have to finish testing the protocol. Stay tuned.

 

[lansbergen]

But if the funding is there and if he doesn't have anything better to do go for it.

Did you read what he is trying to do?

 

[JalapenoLuv]

Yes. His hypothesis is that CFS is an autoimmune disease and that something is triggering B cells to overproduce. I think bartonella spp. infection is a culprit because it blocks B cell apoptosis and macrophage phagocytosis. I wonder if persistent B cells would account for the research he mentioned. I can't look it up because there's no citation. He was turned down by NIH.

 

[MeSci]

Rituximab would be another dead end. Although initially their fatigue would be better, B cells serve a purpose and their long term clinical outcomes wouldn't be any better. In fact, with their fatigue masked they might be worse because they are overtasking their bodies beyond their recuperative abilities.

But if the funding is there and if he doesn't have anything better to do go for it.

There's a lot more to it than that.

I agree that masking fatigue is a bad idea. I also prefer to try natural treatments rather than Rituximab, partly because I am not severely affected and don't want to risk potentially-serious adverse effects (and I research natural treatments fairly thoroughly before trying them, as I know they can have adverse effects too, and I have suffered some).

But I certainly wouldn't dismiss what Prof Edwards is doing, especially in such a disrespectful way. Many people here are very keen to try it, having tried so many other things and often being severely affected. Others are eager to participate in research that might help others, even if they do not benefit personally.

This post by @Jonathan Edwards gives such people some hope.

And as this and some other threads discuss, ME/CFS may be very heterogeneous, so Rituximab could help to distinguish between different subgroups.

 

[JalapenoLuv]

>And as this and some other threads discuss, ME/CFS may be very heterogeneous, so Rituximab could help to distinguish between different subgroups.

That's a good point. Are you aware the longest they've followed patients on it has only been seven months? I wouldn't consent to be a subject.

 

[lansbergen]

Yes. His hypothesis is that CFS is an autoimmune disease and that something is triggering B cells to overproduce. .

He is not trying to separate the wheat from the chaff?

 

[JalapenoLuv]

I'll let him answer, it's his proposal.

 

[Hip]

Methylation also doesn't make sense as an etiology. People are humming along just fine until they get a viral infection then suddenly their cells can't methylate properly? So what's the cause? It can't be environmental or infectious because nobody else is affected. It obviously isn't genetic because they didn't have it previously. It's a stupid theory out of desperation.

You are looking at this too narrowly, and clearly without enough thought.

A lot of ME/CFS patients benefit from the methylation protocol, so it is clear it can help in this disease. How those benefits arise is the question. Methylation may change the expression of genes of the immune system, boosting immunity; so low methylation might make you more susceptible to viruses.

How else might methylation boost the immune response against viruses? Well, Rich van K reckoned insufficient methylation is behind low intracellular glutathione. Now glutathione inhibits calpain in the cell, and it is calpain that is responsible for cutting up the RNase L into small ineffective chunks which lose their antiviral potency, so that they cannot clear viral RNA from cells. I take it you are aware of the low molecular weight RNase L found in ME/CFS. So lack of methylation may prevent the cellular immune system from properly clearing viruses.

You need to do your homework before you call something a stupid theory.

 

[Jonathan Edwards]

I am pleased to hear your input JalapenoLuv, even if to my ears it is mostly a random jumble of incorrect facts. I actually agree with your last post on methylation, even if I did not with the previous one.

I am not sure where you get the seven month follow up from. We have samples in the freezer taken from patients from Norway followed for three years.

Lots of people post some rather doubtful things here but it is a bit of a novelty to have facts so precisely incorrect!

 

[JalapenoLuv]

They should qualify it as a mechanism not a cause of CFS. People can have polymorphisms without having CFS. Can people have CFS without having the polymorphisms? I think so. That's why I reject it.

 

[JalapenoLuv]

I am pleased to hear your input JalapenoLuv, even if to my ears it is mostly a random jumble of incorrect facts. I actually agree with your last post on methylation, even if I did not with the previous one.

I am not sure where you get the seven month follow up from. We have samples in the freezer taken from patients from Norway followed for three years.

Lots of people post some rather doubtful things here but it is a bit of a novelty to have facts so precisely incorrect!

Thanks? I was just going by the published research showing a seven month follow up. Has anything been published showing longer?